A 37-year-old woman, gravida 2 para 1, comes to the emergency department due to painful contractions and leakage of fluid. She has not received prenatal care during this pregnancy and is at 24 weeks gestation by a sure, regular last menstrual period. The patient has no chronic medical conditions. She precipitously delivers a male fetus with no cardiac activity. Examination of the fetus shows edematous, peeling skin. The scalp is edematous, but the palate appears normal and there are no dysmorphic facial features. The fetal abdomen is tense and fluid-filled. The placenta appears thickened and edematous. Maternal laboratory results are as follows:
| Hemoglobin | 11.2 g/dL |
| Blood type | O, Rh negative |
| Indirect Coombs test | negative |
| HIV-1 antibody | negative |
Which of the following is the most likely etiology of this patient's fetal demise?
Fetal hydrops | |
Pathogenesis |
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Clinical features |
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Etiology |
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This fetal demise is most likely due to nonimmune hydrops fetalis (fetal hydrops), a sequela of high-output fetal heart failure characterized by excessive fluid accumulation in interstitial spaces. The most common infectious etiology of hydrops fetalis is maternal parvovirus B19 infection.
Most adults with parvovirus B19 infection are asymptomatic; however, parvovirus B19 during pregnancy can have devastating fetal consequences due to viral cytotoxicity to fetal erythrocyte precursors. With increasingly severe fetal anemia, the fetal heart tries to compensate for hypoxemia by increasing cardiac output. However, eventually it cannot compensate, and high-output fetal heart failure develops. As with other cases of heart failure, fetuses develop third spacing of fluid, resulting in ascites (ie, tense fluid-filled abdomen) and generalized skin edema (and subsequent peeling). Other clinical features include pleural or pericardial effusions and placental edema.
Fetuses with hydrops fetalis are at high risk for fetal demise; this risk increases with infection acquired at earlier gestational ages. Due to this risk, patients with fetal hydrops undergo serial ultrasounds and possible early delivery.
(Choices A and C) Both fetal aneuploidy (eg, trisomy 18) and fetal alcohol spectrum disorder (ie, chronic maternal alcohol use) can have associated congenital cardiac defects (eg, atrioventricular septal defect) that can lead to heart failure and hydrops fetalis. However, these fetuses are typically growth-restricted and have limb abnormalities (eg, shortened long bones, clubfoot) or dysmorphic facial features (eg, hypoplastic midface, flattened nasal bridge). Parvovirus B19 infection is not associated with bony or facial dysmorphic features.
(Choice B) Congenital hypothyroidism can cause swollen, edematous skin (ie, myxedema) due to glycosaminoglycan deposits in the dermis. However, it does not cause ascites or placental edema, making this diagnosis unlikely.
(Choice E) Rh(D) alloimmunization occurs when Rh(D)-negative mothers develop anti-D antibodies from delivering an Rh(D)-positive infant. In subsequent pregnancies, existing maternal anti-D antibodies attack Rh(D)-positive fetal erythrocytes, causing severe anemia and fetal hydrops. Although this patient is Rh(D)-negative, her antibody screen is negative, making this diagnosis unlikely.
Educational objective:
Parvovirus B19 infection in pregnancy can cause severe fetal anemia due to viral cytotoxicity to fetal erythrocyte precursors. Fetal anemia increases cardiac output, which can lead to high-output fetal heart failure, subsequent hydrops fetalis (eg, skin edema, ascites), and possible fetal demise.